Role of the hypothalamic pituitary adrenal axis in the control of the response to stress and infection

The release of adrenocorticotropin (ACTH) from the corticotrophs is controlled principally by vasopressin and corticotropin-releasing hormone (CRH). Oxytocin may augment the release of ACTH under certain conditions, whereas atrial natriuretic peptide acts as a corticotropin release-inhibiting factor to inhibit ACTH release by direct action on the pituitary. Glucocorticoids act on their receptors within the hypothalamus and anterior pituitary gland to suppress the release of vasopressin and CRH and the release of ACTH in response to these neuropeptides. CRH neurons in the paraventricular nucleus also project to the cerebral cortex and subcortical regions and to the locus ceruleus (LC) in the brain stem. Cortical influences via the limbic system and possibly the LC augment CRH release during emotional stress, whereas peripheral input by pain and other sensory impulses to the LC causes stimulation of the noradrenergic neurons located there that project their axons to the CRH neurons stimulating them by alpha-adrenergic receptors. A muscarinic cholinergic receptor is interposed between the alpha-receptors and nitric oxidergic interneurons which release nitric oxide that activates CRH release by activation of cyclic guanosine monophosphate, cyclooxygenase, lipoxygenase and epoxygenase. Vasopressin release during stress may be similarly mediated. Vasopressin augments the release of CRH from the hypothalamus and also augments the action of CRH on the pituitary. CRH exerts a positive ultrashort loop feedback to stimulate its own release during stress, possibly by stimulating the LC noradrenergic neurons whose axons project to the paraventricular nucleus to augment the release of CRH

Neuroprotective effect of ketamine/xylazine on two rat models of Parkinson's disease

There is a great concern in the literature for the development of neuroprotectant drugs to treat Parkinson's disease. Since anesthetic drugs have hyperpolarizing properties, they can possibly act as neuroprotectants. In the present study, we have investigated the neuroprotective effect of a mixture of ketamine (85 mg/kg) and xylazine (3 mg/kg) (K/X) on the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 6-hydroxydopamine (6-OHDA) rat models of Parkinson's disease. The bilateral infusion of MPTP (100 µg/side) or 6-OHDA (10 µg/side) into the substantia nigra pars compacta of adult male Wistar rats under thiopental anesthesia caused a modest (~67%) or severe (~91%) loss of tyrosine hydroxylase-immunostained cells, respectively. On the other hand, an apparent neuroprotective effect was observed when the rats were anesthetized with K/X, infused 5 min before surgery. This treatment caused loss of only 33% of the nigral tyrosine hydroxylase-immunostained cells due to the MPTP infusion and 51% due to the 6-OHDA infusion. This neuroprotective effect of K/X was also suggested by a less severe reduction of striatal dopamine levels in animals treated with these neurotoxins. In the working memory version of the Morris water maze task, both MPTP- and 6-OHDA-lesioned animals spent nearly 10 s longer to find the hidden platform in the groups where the neurotoxins were infused under thiopental anesthesia, compared to control animals. This amnestic effect was not observed in rats infused with the neurotoxins under K/X anesthesia. These results suggest that drugs with a pharmacological profile similar to that of K/X may be useful to delay the progression of Parkinson's disease

A tribute to Samuel MacDonald McCann (1925-2007): in honor of one of the last pioneers of Neuroendocrinology

Submitted by Guilherme Lemeszenski ([email protected]) on 2013-08-22T18:52:46Z No. of bitstreams: 1 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5)Made available in DSpace on 2013-08-22T18:52:46Z (GMT). No. of bitstreams: 1 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) Previous issue date: 2007-05-01Made available in DSpace on 2013-09-30T18:25:13Z (GMT). No. of bitstreams: 2 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) S0100-879X2007000500013.pdf.txt: 7453 bytes, checksum: 19a2782d2d1e9ae1b4a3246afd5bd8f4 (MD5) Previous issue date: 2007-05-01Submitted by Vitor Silverio Rodrigues ([email protected]) on 2014-05-20T13:42:36Z No. of bitstreams: 2 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) S0100-879X2007000500013.pdf.txt: 7453 bytes, checksum: 19a2782d2d1e9ae1b4a3246afd5bd8f4 (MD5)Made available in DSpace on 2014-05-20T13:42:36Z (GMT). No. of bitstreams: 2 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) S0100-879X2007000500013.pdf.txt: 7453 bytes, checksum: 19a2782d2d1e9ae1b4a3246afd5bd8f4 (MD5) Previous issue date: 2007-05-01USP Faculdade de Medicina de Ribeirão Preto Departamento de FisiologiaUSP Faculdade de Odontologia de Ribeirão Preto Departamento de Morfologia, Estomatologia e FisiologiaUNESP Faculdade de Odontologia de Araçatuba Departamento de Apoio, Produção e SaúdeUFRJ Instituto de Biofísica Carlos Chagas FilhoUERJ Instituto de Biologia Departamento de Ciências FisiológicasUFMG ICB Departamento de Fisiologia e BiofísicaUNESP Faculdade de Odontologia de Araçatuba Departamento de Apoio, Produção e Saúd

Decreased spermatogenic and androgenic testicular functions in adult rats submitted to immobilization-induced stress from prepuberty

We investigated whether chronic stress applied from prepuberty to full sexual maturity interferes with spermatogenic and androgenic testicular functions. Male Wistar rats (40 days old) were immobilized 6 h a day for 60 days. Following immobilization, plasma concentrations of corticosterone and prolactin increased 135% and 48%, respectively, while plasma luteinizing hormone and testosterone presented a significant decrease of 29% and 37%, respectively. Plasma concentration of follicle-stimulating hormone was not altered in stressed rats. Chronic stress reduced the amount of mature spermatids in the testis by 16% and the spermatozoon concentration in the cauda epididymidis by 32%. A 17% reduction in weight and a 42% decrease in DNA content were observed in the seminal vesicle of immobilized rats but not in its fructose content. The growth and secretory activity of the ventral prostate were not altered by chronic stress